Abstract:
:In this study, we examined the expression of nerve growth factor (NGF) and its receptors in mouse macrophages and the mechanisms involved in the effect of NGF on tumor necrosis factor (TNF)-alpha production. Macrophages expressed NGF and the NGF receptors TrkA and p75. Treatment of J744 cells or peritoneal macrophages with NGF induced a large increase in the production of TNF-alpha. In addition, NGF induced the secretion of nitric oxide in interferon-gamma-treated J774 cells or lipopolysaccharide-treated peritoneal macrophages. The induction of TNF-alpha production by NGF was blocked by K252a, an inhibitor of the TrkA receptor. NGF induced phosphorylation and activation of extracellular signal-regulated kinase, Erk1/Erk2 and c-Jun amino-terminal kinase, whereas it did not induce phosphorylation of p38 mitogen-activated protein kinase. Inhibition of the MAP kinase-Erk kinase pathway with PD 098059 decreased the secretion of TNF-alpha by NGF. Our results suggest that NGF has an important role in the activation of macrophages during inflammatory responses via activation of mitogen-activated protein kinases.
journal_name
J Leukoc Bioljournal_title
Journal of leukocyte biologyauthors
Barouch R,Kazimirsky G,Appel E,Brodie Csubject
Has Abstractpub_date
2001-06-01 00:00:00pages
1019-26issue
6eissn
0741-5400issn
1938-3673journal_volume
69pub_type
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更新日期:1993-11-01 00:00:00
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pub_type: 杂志文章
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pub_type: 杂志文章,评审
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journal_title:Journal of leukocyte biology
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更新日期:2001-10-01 00:00:00